In incipient heart failure, ventricular hypertrophy is generally considered a compensatory response; however, the precise dynamics of this mechanism have not been defined. The objective of this project is to define the working interrelationships of contractility, load, and wall stress in the intact hypertrophied and decompensated ventricle. The results of these studies are intended to answer the following questions: 1) Is the ventricle subjected to subtle progressive increases in load caused by cardiac dilation? 2) Is stress on the cardiac muscle fiber held constant by increases in wall thickness as force in the ventricular wall increases? 3) Does failure occur when stress on the fiber exceeds the ability of the fiber to contract against it? Finally, 4) Does the failing heart become refractory to digitalis and sympathetic stimulation? In these studies, a series of animals will be subjected to chronic ventricular volume over-load produced by surgical interruption of His bundle. This procedure combined with daily exercise produces hypertrophy of both ventricles and overt heart failure in a high percentage of animals within 3 to 10 months. In one group of animals immediately following production of heart block and in a second control group, four strain guage arches will be attached to the left ventricle for the measurement of contractile force, ventricular size, load and wall thickness. Additionally, aortic and left ventricular pressure will be measured. Wall stress will be estimated as the quotient of load/wall thickness. The response to ouabain and norepinephrine will be recorded. Finally, Frank-Starling curves will be determined. In other animals, these same parameters will be recorded at random times after block with the heart in varying states of hypertrophy and overt failure. It is intended to define the progressive alteration of these parameters during cardiac compensation and development of cardiac failure.